Evidence map›Paper›PMID 36923253›Full record

ReviewFrontiers in cell and developmental biology2023

Updated perspective of EPAS1 and the role in pulmonary hypertension.

Na Wang, Jing Hua, Yuhua Fu, Jun An, Xiangyu Chen, Chuancui Wang, Yanghong Zheng, Feilong Wang, Yingqun Ji, Qiang Li

Open access · goldFull text readReview
In one paragraph

Review in Frontiers in cell and developmental biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
4.1field-weighted citation impact, top 6% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

12 citing papers in PubMed, 16 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Infection and immunity · 2024
    Article
  10. Article
  11. Article
  12. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 4 institutions in 1 country.

Na WangDepartment of Pulmonary and Critical Care Medicine, Shanghai East Hospital Affiliated by Tongji University, Shanghai, China.
Jing HuaDepartment of Pulmonary and Critical Care Medicine, Shanghai East Hospital Affiliated by Tongji University, Shanghai, China.
Yuhua FuDepartment of Pulmonary and Critical Care Medicine, Central Hospital of Jiading District, Shanghai, China.
Jun AnDepartment of Pulmonary and Critical Care Medicine, First Affiliated Hospital of Dalian Medical University, Dalian, China.
Xiangyu ChenDepartment of Pulmonary and Critical Care Medicine, Shanghai East Hospital Affiliated by Tongji University, Shanghai, China.
Chuancui WangDepartment of Pulmonary and Critical Care Medicine, Jinshan Branch of Shanghai Sixth People's Hospital, Shanghai, China.
Yanghong ZhengDepartment of Pulmonary and Critical Care Medicine, Shanghai East Hospital Affiliated by Tongji University, Shanghai, China.
Feilong WangDepartment of Pulmonary and Critical Care Medicine, Shanghai East Hospital Affiliated by Tongji University, Shanghai, China.
Yingqun JiDepartment of Pulmonary and Critical Care Medicine, Shanghai East Hospital Affiliated by Tongji University, Shanghai, China.
Qiang LiDepartment of Pulmonary and Critical Care Medicine, Shanghai East Hospital Affiliated by Tongji University, Shanghai, China.
Shanghai East Hospital · CNDalian Medical University · CNJiading District Central Hospital · CNShanghai Sixth People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pulmonary hypertension (PH) is a group of syndromes characterized by irreversible vascular remodeling and persistent elevation of pulmonary vascular resistance and pressure, leading to ultimately right heart failure and even death. Current therapeutic strategies mainly focus on symptoms alleviation by stimulating pulmonary vessel dilation. Unfortunately, the mechanism and interventional management of vascular remodeling are still yet unrevealed. Hypoxia plays a central role in the pathogenesis of PH and numerous studies have shown the relationship between PH and hypoxia-inducible factors family. EPAS1, known as hypoxia-inducible factor-2 alpha (HIF-2α), functions as a transcription factor participating in various cellular pathways. However, the detailed mechanism of EPAS1 has not been fully and systematically described. This article exhibited a comprehensive summary of EPAS1 including the molecular structure, biological function and regulatory network in PH and other relevant cardiovascular diseases, and furthermore, provided theoretical reference for the potential novel target for future PH intervention.

Indexed as

EPAS1hypoxiapulmonary hypertensiontranscription factorvascular remodeling

Identifiers

PMID36923253
PMCPMC10008962
OpenAlexW4322504167

What Socratic holds

Textfull text, public
LicenceCC BY
reference markers read15
measurements read7
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.